Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

LRG1 is an adipokine that mediates obesity-induced hepatosteatosis and insulin resistance.

ABSTRACT: LRG1 is an adipokine that mediates obesity-induced hepatosteatosis and insulin resistance.

PROVIDER: PRJNA769145 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR16227623.fastq.gz	Fastqsanger.gz
	SRR16227624.fastq.gz	Fastqsanger.gz
	SRR16227625.fastq.gz	Fastqsanger.gz
	SRR16227626.fastq.gz	Fastqsanger.gz
	SRR16227627.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

LRG1 is an adipokine that mediates obesity-induced hepatosteatosis and insulin resistance [array]

Project description:LRG1 is an adipokine that mediates obesity-induced hepatosteatosis and insulin resistance [array]

| PRJNA769184 | ENA

LRG1 is an adipokine that mediates obesity-induced hepatosteatosis and insulin resistance [liver_RNA-seq]

Project description:LRG1 is an adipokine that mediates obesity-induced hepatosteatosis and insulin resistance [liver_RNA-seq]

| PRJNA769183 | ENA

LRG1 is an adipokine that mediates obesity-induced hepatosteatosis and insulin resistance [heaptocyte_RNA-seq]

Project description:LRG1 is an adipokine that mediates obesity-induced hepatosteatosis and insulin resistance [heaptocyte_RNA-seq]

| PRJNA769182 | ENA

LRG1 is an adipokine that mediates obesity-induced hepatosteatosis and insulin resistance [liver_RNA-seq]

Project description:Dysregulation in adipokine biosynthesis and function contributes to obesity-induced metabolic diseases. However, the identities and functions of many of the obesity-induced secretory molecules remain unknown. This study identified Leucine-rich alpha-2-glycoprotein 1 (LRG1) as an obesity-associated adipokine. The effects of LRG1 deficiency on liver tissue gene expression were tested in current assay.

2022-03-04 | GSE185483 | GEO

LRG1 is an adipokine that mediates obesity-induced hepatosteatosis and insulin resistance [heaptocyte_RNA-seq]

Project description:Dysregulation in adipokine biosynthesis and function contributes to obesity-induced metabolic diseases. However, the identities and functions of many of the obesity-induced secretory molecules remain unknown. This study identified Leucine-rich alpha-2-glycoprotein 1 (LRG1) as an obesity-associated adipokine. The effects of LRG1 protein treatment on primary hepatocyte gene expression was tested in current assay.

2022-03-04 | GSE185482 | GEO

LRG1 is an adipokine that mediates obesity-induced hepatosteatosis and insulin resistance [array]

Project description:Dysregulation in adipokine biosynthesis and function contributes to obesity-induced metabolic diseases. However, the identities and functions of many of the obesity-induced secretory molecules remain unknown. In this study, microarray was used to identify genes that are differentially expressed during adipocyte differentiation, further screening based on microarray result identified Leucine-rich alpha-2-glycoprotein 1 (LRG1) as an obesity-associated adipokine. Expression data of pre-adipocytes and mature adipocytes

2022-03-04 | GSE185481 | GEO

LRG1 is an adipokine that promotes insulin sensitivity and suppresses inflammation

Project description:While dysregulation of adipocyte endocrine function plays a central role in obesity and its complications, the vast majority of adipokines remain uncharacterized. We employed bio-orthogonal non-canonical amino acid tagging (BONCAT) and mass spectrometry to comprehensively characterize the secretome of murine visceral and subcutaneous white and interscapular brown adipocytes. Over 600 proteins were identified, the majority of which showed cell type-specific enrichment. We here describe a metabolic role for leucine-rich α-2 glycoprotein 1 (LRG1) as an obesity-regulated adipokine secreted by mature adipocytes. LRG1 overexpression significantly improved glucose homeostasis in diet-induced and genetically obese mice. This was associated with markedly reduced white adipose tissue macrophage accumulation and systemic inflammation. Mechanistically, we found LRG1 binds cytochrome c in circulation to dampen its pro-inflammatory effect. These data support a new role for LRG1 as an insulin sensitizer with therapeutic potential given its immunomodulatory function at the nexus of obesity, inflammation, and associated pathology.

2022-11-21 | PXD035318 | Pride

Removal of visceral adipose tissue prevents obesity-induced multi-organ insulin resistance, dyslipidemia, and NAFLD in mice

Project description:Obesity is associated with insulin resistance, an important risk factor of type 2 diabetes, atherogenic dyslipidemia, nonalcoholic fatty liver disease (NAFLD), and cardiovascular disease. It has been postulated that accumulation of visceral adipose tissue (VAT) causes obesity-induced insulin resistance. The major purpose of this study was to test hypothesis that prophylactic VAT removal prevents the development of obesity-induced multi-organ (liver, skeletal muscle, adipose tissue) insulin resistance, dyslipidemia, and NAFLD. Accordingly, we surgically removed epididymal VAT from adult C57BL/6J mice and then evaluated in vivo and cellular metabolic pathways involved in glucose and lipid metabolism following feeding of chronic high-fat diet (HFD). We found that VAT removal prevented HFD-induced insulin resistance and markedly increased AKT-mediated insulin signaling in subcutaneous adipose tissue (SAT), liver, and skeletal muscle. VAT removal improved plasma lipid profiling and prevented obesity-induced NAFLD. In addition, VAT removal significantly increased circulating level of adiponectin, a key insulin-sensitizing adipokine, whereas it decreased interleukin-6, a pro-inflammatory adipokine. Data obtained from RNA-sequencing suggest that VAT removal prevents obesity-induced oxidative stress and inflammation in liver and SAT respectively. These findings demonstrate the causative role of VAT in the development of obesity and related systemic metabolic complications, such as insulin resistance, dyslipidemia, and NAFLD.

2021-04-01 | GSE157798 | GEO

IL-37 protects against obesity-induced inflammation and insulin resistance

Project description:Cytokines of the IL-1 family are important modulators of obesity-induced inflammation and the development of systemic insulin resistance. Here, we report that IL-37, a newly-described antiinflammatory member of the IL-1 family, affects obesity-induced inflammation and insulin resistance. IL-37 transgenic mice (IL-37tg) did not develop an obese phenotype in response to a high-fat diet (HFD). Unlike WT mice, IL-37tg mice exhibited reduced numbers of adipose tissue macrophages and preserved glucose tolerance and insulin sensitivity after 16 weeks of HFD. A short-term HFD intervention revealed that the IL-37-mediated improvement in glucose tolerance is independent of bodyweight. IL-37tg mice manifested a beneficial metabolic profile with higher circulating levels of the anti-inflammatory adipokine adiponectin. In vitro treatment of differentiating adipocytes with recombinant IL-37 reduced adipogenesis. The beneficial effects of recombinant IL-37 involved activation of AMPK signaling. In humans, steady-state IL-37 adipose tissue mRNA levels were positively correlated with insulin sensitivity, lower adipose tissue levels of leptin and a lower inflammatory status of the adipose tissue. These findings reveal IL-37 as an important anti-inflammatory modulator during obesity-induced inflammation and insulin resistance in both mice and humans and suggest that IL-37 is a potential target for the treatment of obesity-induced insulin resistance and type 2 diabetes. Gene arrays were performed on epidydimal white adipose tissue samples from wild type and human IL37-overexpressing transgenic mice fed a high fat diet for 16 weeks.

2015-05-18 | E-GEOD-58952 | biostudies-arrayexpress

IL-37 protects against obesity-induced inflammation and insulin resistance

2015-05-18 | GSE58952 | GEO